TGF-β and fibrosis in different organs - molecular pathway imprints

被引：579

作者：

Pohlers, Dirk ^{[1
]}

Brenmoehl, Julia ^{[2
]}

Loeffler, Ivonne ^{[3
]}

Mueller, Cornelia K. ^{[4
]}

Leipner, Carola ^{[5
]}

Schultze-Mosgau, Stefan ^{[4
]}

Stallmach, Andreas ^{[2
]}

Kinne, Raimund W. ^{[1
]}

Wolf, Gunter ^{[3
]}

机构：

[1] Univ Jena, Expt Rheumatol Unit, Univ Hosp Jena, Waldkrankenhaus Rudolf Elle Eisenberg,Dept Orthop, Jena, Germany

[2] Univ Jena, Dept Gastroenterol Hepatol & Infect Dis, Clin Internal Med 2, Univ Hosp Jena, Jena, Germany

[3] Univ Jena, Univ Hosp Jena, Clin Internal Med 3, Jena, Germany

[4] Univ Jena, Univ Hosp Jena, Clin Oromaxillofacial Surg Plast Surg, Jena, Germany

[5] Univ Jena, Univ Hosp Jena, Anim Res Inst, Jena, Germany

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2009年 / 1792卷 / 08期

关键词：

TGF-beta; Fibrosis; Arthritis; Nephritis; Inflammatory bowel disease; Crohn's disease; Wound-healing; Myocarditis; GROWTH-FACTOR-BETA; INFLAMMATORY-BOWEL-DISEASE; EPITHELIAL-MESENCHYMAL TRANSITION; B3-INDUCED CHRONIC MYOCARDITIS; SMOOTH MUSCLE ACTIN; COLLAGEN-INDUCED ARTHRITIS; MATRIX GENE-EXPRESSION; PROXIMAL TUBULAR CELLS; FOCAL ADHESION KINASE; TUMOR-NECROSIS-FACTOR;

D O I：

10.1016/j.bbadis.2009.06.004

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

The action of transforming-growth-factor (TGF)-beta following inflammatory responses is characterized by increased production of extracellular matrix (ECM) components, as well as mesenchymal cell proliferation, migration, and accumulation. Thus, TGF-beta is important for the induction of fibrosis often associated with chronic phases of inflammatory diseases. This common feature of TGF-related pathologies is observed in many different organs. Therefore, in addition to the description of the common TGF-beta-pathway, this review focuses on TGF-beta-related pathogenetic effects in different pathologies/organs, i.e., arthritis, diabetic nephropathy, colitis/Crohn's disease, radiation-induced fibrosis, and myrocarditis (including their similarities and dissimilarities). However, TGF-beta exhibits both exacerbating and ameliorating features, depending on the phase of disease and the site of action. Due to its central role in severe fibrotic diseases, TGF-beta nevertheless remains an attractive therapeutic target, if targeted locally and during the fibrotic phase of disease. (C) 2009 Elsevier B.V. All rights reserved.

引用

页码：746 / 756

页数：11

共 185 条

[1]

Transforming growth factor-β1 is up-regulated by podocytes in response to excess intraglomerular passage of proteins -: A central pathway in progressive glomerulosclerosis [J].

Abbate, M ;

Zoja, C ;

Morigi, M ;

Rottoli, D ;

Angioletti, S ;

Tomasoni, S ;

Zanchi, C ;

Longaretti, L ;

Donadelli, R ;

Remuzzi, G .

AMERICAN JOURNAL OF PATHOLOGY, 2002, 161 (06) :2179-2193

[2]

RAPID ONSET SYNOVIAL INFLAMMATION AND HYPERPLASIA INDUCED BY TRANSFORMING GROWTH FACTOR-BETA [J].

ALLEN, JB ;

MANTHEY, CL ;

HAND, AR ;

OHURA, K ;

ELLINGSWORTH, L ;

WAHL, SM .

JOURNAL OF EXPERIMENTAL MEDICINE, 1990, 171 (01) :231-247

[3]

Making sense of latent TGFβ activation [J].

Annes, JP ;

Munger, JS ;

Rifkin, DB .

JOURNAL OF CELL SCIENCE, 2003, 116 (02) :217-224

[4]

[Anonymous], 1998, CURR PR MED

[5]

Imatinib as a novel antifibrotic agent in bleomycin-induced pulmonary fibrosis in mice [J].

Aono, Y ;

Nishioka, Y ;

Inayama, M ;

Ugai, M ;

Kishi, J ;

Uehara, H ;

Izumi, K ;

Sone, S .

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2005, 171 (11) :1279-1285

[6]

Epithelial mesenchymal interactions in cancer and development [J].

Arias, AM .

CELL, 2001, 105 (04) :425-431

[7]

The compliance of collagen gels regulates transforming growth factor-β induction of α-smooth muscle actin in fibroblasts [J].

Arora, PD ;

Narani, N ;

McCulloch, CAG .

AMERICAN JOURNAL OF PATHOLOGY, 1999, 154 (03) :871-882

[8]

Expression of transforming growth factors alpha and beta in colonic mucosa in inflammatory bowel disease [J].

Babyatsky, MW ;

Rossiter, G ;

Podolsky, DK .

GASTROENTEROLOGY, 1996, 110 (04) :975-984

[9]

Growth factors in inflammatory bowel disease [J].

Beck, PL ;

Podolsky, DK .

INFLAMMATORY BOWEL DISEASES, 1999, 5 (01) :44-60

[10]

Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells [J].

Bettelli, E ;

Carrier, YJ ;

Gao, WD ;

Korn, T ;

Strom, TB ;

Oukka, M ;

Weiner, HL ;

Kuchroo, VK .

NATURE, 2006, 441 (7090) :235-238

← 1 2 3 4 5 6 7 8 9 10 →